Endocardial Mapping Research Articles

Real-time correction of respiratory-induced cardiac motion during electroanatomical mapping procedures.

Treatment planning during catheter interventions in the heart is often based on electromechanical tissue characteristics obtained by endocardial surface mapping (ESM). Since studies have shown respiratory-induced cardiac motion of over 5 mm in different directions, respiratory motion may cause ESMs artifacts due to faulty interpolation. Hence, we designed and tested a real-time respiration-correction algorithm for ESM. An experimental phantom was used to design the correction algorithm which was subsequently evaluated in five pigs. A piezo-respiratory belt transducer was used to measure the respiration. The respiratory signal was inserted to the NOGA®XP electromechanical mapping system via the ECG leads. The results of the correction were assessed by measuring the displacement of a reference point and the registration error of the ESM on a CMR scan before and after correction. In the phantom experiment, the reference point displacement was 6.5 mm before and 1.1 mm after correction and the registration errors were 2.8 ± 2.2 and 1.9 ± 1.3 mm, respectively. In the animals, the average reference point displacement (apex) was reduced from 2.6 ± 1.0 mm before to 1.2 ± 0.3 mm after correction (P < 0.05). The in vivo registration error of the ESM and the CMR scan did not significantly improve. Even though the apical movement appreciated in pigs is small, the correction algorithm shows a decrease in displacement after correction. Application of this algorithm omits the use of the time-consuming respiratory gating during ESM and may lead to less respiratory artifacts in clinical endocardial mapping procedures.

Investigating a Novel Activation-Repolarisation Time Metric to Predict Localised Vulnerability to Reentry Using Computational Modelling

Exit sites associated with scar-related reentrant arrhythmias represent important targets for catheter ablation therapy. However, their accurate location in a safe and robust manner remains a significant clinical challenge. We recently proposed a novel quantitative metric (termed the Reentry Vulnerability Index, RVI) to determine the difference between activation and repolarisation intervals measured from pairs of spatial locations during premature stimulation to accurately locate the critical site of reentry formation. In the clinic, the method showed potential to identify regions of low RVI corresponding to areas vulnerable to reentry, subsequently identified as ventricular tachycardia (VT) circuit exit sites. Here, we perform an in silico investigation of the RVI metric in order to aid the acquisition and interpretation of RVI maps and optimise its future usage within the clinic. Within idealised 2D sheet models we show that the RVI produces lower values under correspondingly more arrhythmogenic conditions, with even low resolution (8 mm electrode separation) recordings still able to locate vulnerable regions. When applied to models of infarct scars, the surface RVI maps successfully identified exit sites of the reentrant circuit, even in scenarios where the scar was wholly intramural. Within highly complex infarct scar anatomies with multiple reentrant pathways, the identified exit sites were dependent upon the specific pacing location used to compute the endocardial RVI maps. However, simulated ablation of these sites successfully prevented the reentry re-initiation. We conclude that endocardial surface RVI maps are able to successfully locate regions vulnerable to reentry corresponding to critical exit sites during sustained scar-related VT. The method is robust against highly complex and intramural scar anatomies and low resolution clinical data acquisition. Optimal location of all relevant sites requires RVI maps to be computed from multiple pacing locations.

Electroanatomic Correlates of Depolarization Abnormalities in Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy.

Epsilon waves and other depolarization abnormalities in the right precordial leads are thought to represent delayed activation of the right ventricular outflow tract in arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C). However, no study has directly correlated cardiac electrical activation with the surface ECG findings in ARVD/C. Thirty ARVD/C patients (mean age 32.7 ± 11.2years, 16 men) underwent endocardial and epicardial electroanatomical activation mapping in sinus rhythm. Twelve-lead ECGs were classified into 5 patterns: (1) normal QRS (11 patients); (2) terminal activation delay (TAD) (3 patients); (3) incomplete right bundle branch block (IRBBB) (5 patients); (4) epsilon wave (5 patients); (5) complete right bundle branch block (CRBBB) (6 patients). Timing of local ventricular activation and extent of scar was then correlated with surface QRS. Earliest endocardial and epicardial RV activation occurred on the mid anteroseptal wall in all patients despite the CRBBB pattern on ECG. Total RV activation times increased from normal QRS to prolonged TAD, IRBBB, epsilon wave, and CRBBB, respectively (103.9 ± 5.6, 116.3 ± 6.5, 117.8 ± 2.7, 146.4 ± 16.3, and 154.3 ± 6.3, respectively, P < 0.05). The total epicardial scar area (cm(2) ) was similar among the different ECG patterns. Median endocardial scar burden was significantly higher in patients with epsilon waves even compared with patients with CRBBB (34.3 vs. 11.3 cm(2) , P < 0.01). Timing of epsilon wave corresponded to activation of the subtricuspid region in all patients. We found that epsilon waves are often associated with severe conduction delay and extensive endocardial scarring in addition to epicardial disease. The timing of epsilon waves on surface ECG correlated with electrical activation of the sub-tricuspid region.

Difference in the maintenance mechanism of atrial fibrillation perpetuated after pulmonary vein isolation between paroxysmal and persistent atrial fibrillation: Effects of subsequent stepwise ablation

BackgroundNeither the atrial fibrillation (AF) maintenance mechanism after pulmonary vein isolation (PVI) nor the mechanism of AF termination via stepwise ablation is clearly understood. MethodsAmong 226 consecutive AF patients (154 paroxysmal (P-AF) and 72 persistent AF (Per-AF) patients), left atrial endocardial non-contact mapping was performed after PVI in the initial 10 P-AF and 16 Per-AF patients to define the AF maintenance mechanism. Subsequently, effect of stepwise catheter ablation (linear roof lesion and complex fractionated atrial electrogram (CFAE) following PVI) was evaluated in all patients. ResultsAfter PVI, AF was maintained by the activation around isolated PV/mitral annulus, focal discharge and disorganized activations mostly observed over residual CFAE region (pivoting activation, wave break and fusion). CFAE region in P-AF was smaller than Per-AF after PVI (1.6±2.1 vs. 7.7±2.5cm2, p<0.0001). The frequency of pivoting activation, wave break and fusion in P-AF were lower than those in Per-AF (1.9±2.0 vs. 11.8±5.0 times/s; p<0.0001, 0.1±0.3 vs. 3.6±2.5 times/s; p<0.001, 5.8±3.6 vs. 9.8±3.2 times/s; p<0.01). AF termination was more frequent in P-AF than Per-AF (94.8% vs 81.9%, p=0.0019). AF termination by PVI alone was more frequent in P-AF than Per-AF (85.6% vs. 18.6%, p<0.0001). However, AF termination via roof line and/or CFAE ablation was less frequent in P-AF than Per-AF (14.4 vs. 81.4%, p<0.0001). ConclusionsDisorganized activations after PVI, more prominent in Per-AF, were associated with residual CFAE region. Most P-AF was terminated by PVI alone, however additional roof line lesion and CFAE ablation were necessary to terminate Per-AF, consistent with mapping results.

Spatial Relationship of Focal Impulses, Rotors and Low Voltage Zones in Patients With Persistent Atrial Fibrillation.

Focal impulses (FI) and rotors are sources associated with the initiation and maintenance of atrial fibrillation (AF). Their ablation results in a lower recurrence rate. The aim of this study was to characterize for the first time the spatial relationship between such sources and atrial low voltage zones (LVZ) representing fibrosis. Twenty-five consecutive patients undergoing their first ablation for persistent AF were included. Voltage mapping of both atria was done during AF. Endocardial mapping of FI and rotors (sources) was performed using a basket catheter and displayed using RhythmView(TM) (Topera Inc.) before ablation. Spatial relationship of LVZ and sources was analyzed. LVZs covered 13 ± 12% of right atrial (RA) endocardial surface and 33 ± 25% of left atrial (LA) endocardial surface. The median number of sources was 1 [1-3] in RA and 3 [1-4] in LA. Of LA sources, 18 (30%) were definitely not associated with LVZs or pulmonary vein (PV) antra. Of RA sources, 32 (84%) were remote from LVZ. During ablation of such sources substantial cycle length (CL) prolongation or AF conversion occurred in 11/23 patients (48%). Altogether, 8/11 (73%) of these pertinent sources were located remotely from LVZ and PV antra. There is a wide discrepancy in distribution of LVZ areas and sites of identified rotors. Site and incidence of FIRM sources appear to be unpredictable with atrial substrate mapping. Further prospective, randomized studies are necessary to elucidate the impact of additional ablation of such sources in patients with persistent or longstanding persistent AF.

Analysis of Activation-Recovery Intervals from Intracardiac Electrograms in Normal and Infarcted Porcine Hearts

Mapping of intracardiac electrical signals is a well-established clinical method used to identify the foci of abnormal heart rhythms associated with chronic myocardial infarct (a major cause of death). These foci reside in the ‘border zone’ (BZ) between healthy tissue and dense collagenous scar, and are the targets of ablation therapy. In this work we analyzed detailed features of the electrical signals recorded in a translational animal model of chronic infarct. Specifically, three-dimensional activation maps and bipolar voltages were recorded in vivo from 8 pigs at 5-6 weeks following infarct creation, as well as 7 control (normal) pigs. Endocardial and epicardial maps were obtained during normal sinus rhythm and/or pacing conditions via a catheter-based electro-anatomical CARTO-XP mapping system (Biosense, Webster). Next, depolarization and repolarization maps were derived through manual annotation of electro-cardiogram waves, where the peak of the QRS wave marked the time of depolarization and the peak of the T wave marked the recovery time. Then, at each recording point, activation-recovery intervals (ARI) were found by subtracting activation times from repolarization times. Such ARI maps are important clinical surrogates of action potential duration. Overall, we observed that ARI values in the BZ have recovered from the acute stage and were close to ARI values in normal tissue. Furthermore, in both infarcted and normal cases we observed: i) a weak negative correlation between the activation times and ARI values, and ii) not a significant variation (p<0.5) between mean ARI values in the BZ area and those in the healthy areas. Our future work will focus on personalizing mathematical models from these electrical maps per individual hearts, to enable accurate predictions of cardiac wave propagation and the inducibility of scar-related abnormal rhythms.

The effect of electrode density on the interpretation of atrial activation patterns in epicardial mapping of human persistent atrial fibrillation

Mechanisms sustaining human persistent atrial fibrillation (AF) remain debated, with significant differences between high-density epicardial and global endocardial mapping studies. A key difference is the density of recording electrodes. We aimed to determine the differences in the prevalence of different atrial activation patterns, and specifically in the prevalence of rotational activations, with varying densities of bipolar electrodes. Epicardial mapping was performed in 10 patients undergoing cardiac surgery, with bipolar electrograms recorded using a triangular plaque (6.75 cm(2) area; 117 bipoles; 2.5-mm inter-bipole spacing) applied to the left atrial posterior wall or right atrial free wall. Dynamic wavefront mapping based on the timing of atrial electrograms was applied to 2 discrete 10-second AF segments. The spacing between bipolar electrode locations was increased from 2.5 × 3.5 mm in the horizontal and oblique directions to 5.0 × 3.5, 5.0 × 7.1, and 7.5 × 10.6 mm, with wavefront mapping repeated at each density. As density reduced, there was a significant change in relative proportions of the various activation patterns (F=3.69; P < .001). Simple broad wavefront activations became more prevalent (20% ± 8% to 54% ± 8%; P < .05) and complex patterns became less prevalent (48% ± 8% to 9% ± 8%; P < .05) with reducing density. The prevalence of rotational activity declined with bipole density, from median 5.0% (range 0.9%-12.1%) to 0% (range 0%-1.5%) (P = .03). The largest change occurred between inter-bipole spacings of 5.0 × 3.5 and 5.0 × 7.1 mm. Apparent activation patterns in persistent AF vary significantly with electrode density. Low density underestimates the prevalence of complex and rotational patterns. The largest difference occurs between an inter-bipole spacing of 5.0 × 3.5 and a spacing of 5.0 × 7.1 mm. This may have important implications for mapping technology design.

QRS Fragmentation Outcome in Patients Receiving Cardiac Resynchronization Therapy

Background: Myocardial scar causes heterogeneous ventricular activation, which results in the fragmentation of QRS (f-QRS) com- plexes. Objectives: The current study aimed to investigate the clinical and echocardiographic benefits of cardiac resynchronization therapy (CRT) implantation in patients with f-QRS versus the patients without it. Patients and Methods: Eighty patients (40 with and 40 without f-QRS) who underwent CRT were enrolled and followed up for six months. The two groups were compared for the functional class, quality of life, echocardiography indices, arrhythmia burden, recur- rent hospitalization and mortality before and after CRT implantation. Results: The mean baseline left ventricular ejection fraction (LVEF), left ventricular end diastolic dimension (LVEDD) and left ventricular end systolic dimension (LVESD) in both groups were not dierent (P > 0.05). Improvements were observed in LVESD, LVEDD and LVEF in patients without f-QRS after CRT (P = 0.003). The functional class and mitral regurgitation (MR) severity improved in both groups. Before implantation, 36 (45%) and 27 (33.8%) patients had mild and moderate MR, respectively. Six months post implantation, 41 (51%) (17 cases with f-QRS) and 20 (25%) (11 cases with f-QRS) patients had mild and moderate MR, respectively (P = 0.003). Improvements in the MR severity and functional class were observed in both groups. Conclusions: Regarding LVEF, LVESD, and LVEDD, a significant dierence was observed in patients without f-QRS after CRT implantation 1. Background Electrical dyssynchrony is present when a wide QRS is evident on electrocardiography (ECG). In a subset of pa- tients with heart failure (HF) and reduced left ventricular ejection fraction (LVEF), this dyssynchrony contributes to the pathophysiology of HF and is associated with negative remodeling and increased risk of clinical events, including mortality. In the majority of HF patients with evidence of dyssynchrony, cardiac resynchronization therapy (CRT) re- stores the appropriate timing of the cardiac contraction and thereby not only reduces cellular, hemodynamic and structural maladaptations of dyssynchrony, but also ulti- mately improves functional status, decreases hospitaliza- tion, and increases survival. Slurring and changes in the morphology of the QRS complex are investigated since the 1960s. Das et al. (1) demonstrated that the presence of fragmented QRS (f- QRS) complexes was more common among patients with prior myocardial infarction and among patients with ei- ther right or left ventricular (LV) enlargement. The f-QRS, in particular late potentials, is investigated as a possi- ble new tool to identify the high-risk cardiac population. Upon the analysis of the data obtained from an epicar- dial and endocardial mapping of the patients undergoing LV aneurysm incision, Pietrasik (2) demonstrated that a fragmented electrical activity was present in all patients with LV aneurysms. However, the patients with ventricu- lar tachycardia had the fragmented electrical activity from a larger proportion of the endocardial border zone and had more prolonged electrogram in this zone than pa- tients without ventricular tachycardia. It was proposed that the endocardial electrical activity mapping and detec- tion of the fragmented activity was a useful tool for surgi- cally guided therapy in ventricular aneurysm and ventric- ular tachycardia (3).

0340: Initial experience with ultra-high density electroanatomical mapping for arrhythmias

We report our initial experience with the newly released ultra-high density (UHD) electroanatomical mapping system (Rhythmia, Boston Scientific) for arrhythmias. All procedures using the multielectrodes catheter (Orion, Boston Scientific) in our institution, for arrhythmias mapping were analyzed. Procedure and fluoroscopy times were also assessed. 20 patients were included (67,9±13 y) for radiofrequency ablation of accessory pathway (n=2) / typical flutter (n=5) / atrial fibrillation (AF n=2) / post-AF ablation left atrial tachycardia (AT n=6) / focal AT (n=2)/ left and right ventricular ectopies (n=3). 63 maps (3,15 maps per patient) were acquired within a mean mapping time of 18±10min per map, including a mean number of 10024,3±9371 electrograms per map (Figure): RA maps (flutter=12; sinus rhythm SR=14; coronary sinus CS pacing=4); left atrial maps (during tachycardia=18; SR=3; CS pacing=4); right ventricular maps (n=4); left ventricular maps (during tachycardia=3; pacing=1). Acute success was achieved in 19/20 patients. In one patient, the ablation could not be performed in the absence of clinical ectopies. Total procedure and fluoroscopy times were respectively 232±78min and 15,9±8 min. No periprocedural complications were noticed. UHD electroanatomical endocardial mapping can be safely performed in both atria and ventricles and allows fast and accurate mapping. Abstract 0340 – Figure: Ultra high density left atrial macro reentry map

To implant or not to implant? : That is the unsolved question concerning heart failure patients with non-LBBB.

To implant or not to implant? : That is the unsolved question concerning heart failure patients with non-LBBB.

Abstract 18572: Limitations of Endocardial Unipolar Voltage Mapping in Predicting the Epicardial Substrate

Introduction: Bipolar voltage mapping detects areas of scar and guides ablation of VT. The role of endocardial unipolar voltage mapping is not well defined. We examined the endo-epicardial substrate in a mixed cohort of patients with structural heard disease (SHD) to determine whether an endocardial unipolar low voltage area predicts the presence and location of an epicardial scar. Results: Data from 24 consecutive patients with SHD (11 ICM, 6 NICM, 3 HCM, 2 ARVC, 1 myocarditis, 1 Brugada) with a detailed (mean points per map 200) combined endocardial-epicardial substrate mapping were retrospectively reviewed. Maps were obtained using a 3D mapping system (CARTO 3) and normal thresholds used were ≤1.5 mV for bipolar voltage, and ≤5.5 (RV) or ≤8.3 mV (LV) for unipolar voltage. Mapping was performed in the LV in 17 patients, in the RV in 6 patients, in both in 1 patient. An endocardial unipolar low voltage area was found in 21/25 maps. In 12/21 maps there was no corresponding epicardial scar, while in 3/4 cases an epicardial scar was detected despite a negative unipolar map (PPV=43%, NPV=25%, P=NS; Fig. 1). In the 9 cases with both positive endocardial unipolar and epicardial bipolar maps, the epicardial scar was found in the corresponding ventricular region of the endocardial low-voltage area, although unipolar area had a tendency to overestimate the area of the scar (115 vs 95 cm 2 ). Conclusion: In this series of patients with SHD, analysis of unipolar voltage maps could not reliably predict the epicardial arrhythmogenic substrate. There is a modest correlation between areas of endocardial unipolar low voltage and epicardial scars (57% of patients with an abnormal unipolar map had a normal epicardial substrate). Moreover, an epicardial substrate cannot be safely excluded based on a normal unipolar endocardial map. Fig. 1 Abnormal bipolar epicardial map (left) with corresponding normal unipolar endocardial map (right) in a patient with ARVC. Pink dots represent area of defragmentation.

Abstract 16807: Role of Rotor Activation Within the Pulmonary Vein as the Driving Sources for Atrial Fibrillation: Three-dimensional Analysis using a Non-contact Mapping System

Background: It has been suggested rotor which is located within the pulmonary vein (PV) acted as the driving sources of atrial fibrillation (AF). However, it has never been confirmed whether or not the rotor exists within PV in human. Objectives: We analyzed the activation sequence within the PV during AF and examined how the PV acted as the driving sources of AF. Methods: Selective endocardial mapping of left superior PV (LSPV) was performed during AF in 11 paroxysmal AF patients using a non-contact mapping system (EnSite 3000). Presence of rotor activation was defined when the circular activation around the functional block line once completed its whole reentrant activation. We analyzed the relation between the pivoting activation and the rotor activation. To define the preferable site of rotor and pivoting activation, we also analyzed the relation between the location of rotor and pivoting activation and region of the complex fractionated electrogram (CFE) recording site. Results: Rotor activation was observed with a mean number of 4.6±3.6 times/sec. CFE was observed at the roof (n=5), ridge (n=11) and carina (n=7) of the proximal half of LSPV with a mean area of 9.1±3.4 cm2. The number of rotor activation observed at the CFE area was significantly higher than that at the non-CFE area (4.1±3.9 vs. 0.7±1.2 times/sec, p=0.025). Total frequency of pivoting activation was 37.0±14.7 times/sec. Pivoting activation involved in the rotor activation was significantly lower than that not involved in the rotor activation (8.8±8.1 vs. 27.7±15.8 times/sec, p=0.0116). Regarding the CFE area, pivoting activation involved in the rotor activation was also significantly lower than that not involved in the rotor activation (8.4±8.2 vs. 24.1±12.0 times/sec, p=0.0105). However, there was no difference between the frequencies of pivoting activation with and without rotor activation in the non-CFE area (1.0±2.0 vs. 3.6±6.1 times/sec, p=NS). Conclusions: Rotor activation was observed at the proximal portion of the LSPV coincided with the location of CFE area. However, most of pivoting activation was not involved in the rotor activation. These suggest that AF was driven by the other meandering propagation associated with frequent non-stable pivoting activation over the CFE area.

Abstract 16789: Activation Sequence within the Pulmonary Vein as the Driving Sources of Atrial Fibrillation: Three-dimensional Analysis Using a Non-contact Mapping System

Background: The mechanisms how the activation within the pulmonary vein (PV) drives the atrial fibrillation (AF) has not been elucidated. Objectives: To define the AF maintenance mechanism by PV, we analyzed the activation sequence within the PV during AF. Methods: Selective endocardial mapping of the left superior PV (LSPV) was performed during AF in 11 patients with paroxysmal AF using a three-dimensional non-contact mapping system (EnSite 3000). In addition, we analyzed how the circumferential radiofrequency energy applications around the LSPV alter the activation of the LSPV and terminate AF. Results: Complex fractionated electrograms (CFE) were observed at the second half of the proximal LSPV at the roof (n=5), ridge (n=11) and carina (n=7). Mean CFE area was 9.1±3.4 cm2, which occupied the 19.8% of the LSPV area. Frequent episodes of pivoting activation associated with wave break and fusion was observed at this CFE area. The frequency of pivoting activation around the functional conduction block, wave break and fusion at the CFE region were significantly higher than those at the non-CFE region (32.5±12.2 vs. 4.6±5.8 times/sec; p&lt;0.0001, 9.2±5.1 vs. 1.4±3.1 times/sec; p=0.0007, and 12.9±4.8 vs. 6.4±4.4 times/sec, p=0.0044). After isolation of ipsilateral right PV, subsequent circumferential radiofrequency energy applications around the left PV terminate the AF with a mean number of 13.5±7.8 applications, including LSPV roof (n=3.0±2.2) and LSPV ridge (n=5.6±1.9) lesions. AF was terminated before left PV isolation in all patients. The frequency of pivoting activation, wave break and fusion at all PV area just before the AF termination were significantly lower than those before ablation (8.1±11.7 vs. 37.0±14.7 times/sec; p&lt;0.0001, 2.3±5.8 vs. 10.6±6.6 times/sec; p=0.005, 6.9±6.8 vs. 19.3±7.1 times/sec, p=0.0004), suggesting that linear lesion eliminate the random wave propagation over the CFE area. Conclusions: AF was driven by the high frequent episodes of pivoting activation associated with wave break and wave fusion observed over the CFE area at the proximal PV. Linear lesions along the left PV including CFE area of the LSPV eliminate the meandering activation over the CFE area, resulting in the termination of AF.

HALT & REVERSE: Hsf1 activators lower cardiomyocyt damage; towards a novel approach to REVERSE atrial fibrillation.

BackgroundAtrial fibrillation is a progressive arrhythmia, the exact mechanism underlying the progressive nature of recurrent AF episodes is still unknown. Recently, it was found that key players of the protein quality control system of the cardiomyocyte, i.e. Heat Shock Proteins, protect against atrial fibrillation progression by attenuating atrial electrical and structural remodeling (electropathology). HALT & REVERSE aims to investigate the correlation between electropathology, as defined by endo- or epicardial mapping, Heat Shock Protein levels and development or recurrence of atrial fibrillation following pulmonary vein isolation, or electrical cardioversion or cardiothoracic surgery.Study designThis study is a prospective observational study. Three separate study groups are defined: (1) cardiothoracic surgery, (2) pulmonary vein isolation and (3) electrical cardioversion. An intra-operative high-resolution epicardial (group 1) or endocardial (group 2) mapping procedure of the atria is performed to study atrial electropathology. Blood samples for Heat Shock Protein determination are obtained at baseline and during the follow-up period at 3 months (group 2), 6 months (groups 1 and 2) and 1 year (group 1 and 2). Tissue samples of the right and left atrial appendages in patients in group 1 are analysed for Heat Shock Protein levels and for tissue characteristics. Early post procedural atrial fibrillation is detected by continuous rhythm monitoring, whereas late post procedural atrial fibrillation is documented by either electrocardiogram or 24-h Holter registration.ConclusionHALT & REVERSE aims to identify the correlation between Heat Shock Protein levels and degree of electropathology. The study outcome will contribute to novel diagnostic tools for the early recognition of clinical atrial fibrillation.Trial Registrations: Rotterdam Medical Ethical Committee MEC-2014-393, Dutch Trial Registration NTR4658

Age-Related Electrophysiological Changes of the Atrial Myocardium in Patients with Paroxysmal Atrial Fibrillation

The process of aging and its effect on the histological appearance of the conduction system of the heart have been scantly described. It is not easy to attribute a certain condition to the aging process because it is often impossible to separate physiological aging from the development of pathological changes due to a concomitant disease. Nevertheless, the fact is that atrial fibrillation (AF) is a common arrhythmia in the elderly, and its incidence rise sharply with age. The increase in prevalence of AF in older persons has been reported to be associated with degeneration of the atrial muscle in pathological studies. Evidence in the human atrial muscle of age-related electrical uncoupling of the side-to-side connections between bundles, related to the proliferation of extensive collagenous tissue septa in intracellular spaces was clearly demonstrated. This translates into electrophysiological changes, hence prolonged and fractionated atrial electrograms are recorded from these areas during sinus rhythm by endocardial mapping of the atrium. These abnormal atrial electrograms are characteristics of paroxysmal AF and were found in a significantly greater proportion in older patients than in younger ones with AF. Advancing age is associated with atrial remodeling characterized by anatomical and structural changes, reductions in atrial voltage with discrete areas of fractionated and prolonged atrial endocardial electrograms, widespread conduction slowing as well as anatomically determined functional conduction delay and block. These electrophysiological changes within the atrial myocardium may be responsible substrate for the increased propensity to develop AF with increasing age.

Transbaffle catheter ablation of atrial re-entrant tachycardia within the pulmonary venous atrium in adult patients with congenital heart disease.

Catheter ablation of atrial re-entrant tachycardia in patients after atrial switch procedure for transposition of the great arteries or with a Fontan circulation is technically challenging if the critical part of the re-entry circuit is located within the pulmonary venous atrium (PVA). We report our experience in transbaffle access (TBA) to the PVA for ablation of atrial re-entrant tachycardia focusing on technical details. In eight patients, six after Mustard procedure and two with a Fontan circulation, endocardial mapping of atrial re-entrant tachycardia revealed the critical part of the re-entry circuit within the PVA. A total of 10 ablation procedures were performed. Detailed angiographic assessment of the anatomy of the systemic and pulmonary venous atria was performed prior to baffle puncture. Transbaffle access was successfully established with a standard transseptal needle in 9 of 10 procedures. No major complications occurred. At the end of the procedure and the removal of the transseptal sheath, there was no residual shunt in any patient. Transbaffle access to the PVA for ablation of atrial re-entrant tachycardia is feasible, less invasive than alternative approaches and can be safely applied in patients after Mustard procedure or with a Fontan circulation. However, the rigidity of prosthetic material may preclude baffle puncture at least in a subset of those patients.

Pericardial adhesions as a consequence of cryoballoon ablation detected during the hybrid AF ablation procedure

Pericardial adhesions as a consequence of cryoballoon ablation detected during the hybrid AF ablation procedure

ST-Segment Elevation and Fractionated Electrograms in Brugada Syndrome Patients Arise From the Same Structurally Abnormal Subepicardial RVOT Area but Have a Different Mechanism.

Brugada syndrome (BrS) is characterized by a typical ECG pattern. We aimed to determine the pathophysiologic basis of the ST-segment in the BrS-ECG with data from various epicardial and endocardial right ventricular activation mapping procedures in 6 BrS patients and in 5 non-BrS controls. In 7 patients (2 BrS and 5 controls) with atrial fibrillation, an epicardial 8×6 electrode grid (interelectrode distance 1 mm) was placed epicardially on the right ventricular outflow tract (RVOT) before video-assisted thoracoscopic surgical pulmonary vein isolation. In 2 other BrS patients, endocardial, epicardial RV (CARTO), and body surface mapping was performed. In 2 additional BrS patients, we performed decremental preexcitation of the RVOT before endocardial RV mapping. During video-assisted thoracoscopic surgical pulmonary vein isolation and CARTO mapping, BrS patients (n=4) showed greater activation delay and more fractionated electrograms in the RVOT region than controls. Ajmaline administration increased the region with fractionated electrograms, as well as ST-segment elevation. Preexcitation of the RVOT (n=2) resulted in ECGs that supported the current-to-load mismatch hypothesis for ST-segment elevation. Body surface mapping showed that the area with ST-segment elevation anatomically correlated with the area of fractionated electrograms and activation delay at the RVOT epicardium. ST-segment elevation and epicardial fractionation/conduction delay in BrS patients are most likely related to the same structural subepicardial abnormalities, but the mechanism is different. ST-segment elevation may be caused by current-to-load mismatch, whereas fractionated electrograms and conduction delay are expected to be caused by discontinuous conduction in the same area with abnormal myocardium.

Rapid automatic segmentation of abnormal tissue in late gadolinium enhancement cardiovascular magnetic resonance images for improved management of long-standing persistent atrial fibrillation.

BackgroundAtrial fibrillation (AF) is the most common heart rhythm disorder. In order for late Gd enhancement cardiovascular magnetic resonance (LGE CMR) to ameliorate the AF management, the ready availability of the accurate enhancement segmentation is required. However, the computer-aided segmentation of enhancement in LGE CMR of AF is still an open question. Additionally, the number of centres that have reported successful application of LGE CMR to guide clinical AF strategies remains low, while the debate on LGE CMR’s diagnostic ability for AF still holds. The aim of this study is to propose a method that reliably distinguishes enhanced (abnormal) from non-enhanced (healthy) tissue within the left atrial wall of (pre-ablation and 3 months post-ablation) LGE CMR data-sets from long-standing persistent AF patients studied at our centre.MethodsEnhancement segmentation was achieved by employing thresholds benchmarked against the statistics of the whole left atrial blood-pool (LABP). The test-set cross-validation mechanism was applied to determine the input feature representation and algorithm that best predict enhancement threshold levels.ResultsGlobal normalized intensity threshold levels TPRE = 1 1/4 and TPOST = 1 5/8 were found to segment enhancement in data-sets acquired pre-ablation and at 3 months post-ablation, respectively. The segmentation results were corroborated by using visual inspection of LGE CMR brightness levels and one endocardial bipolar voltage map. The measured extent of pre-ablation fibrosis fell within the normal range for the specific arrhythmia phenotype. 3D volume renderings of segmented post-ablation enhancement emulated the expected ablation lesion patterns. By comparing our technique with other related approaches that proposed different threshold levels (although they also relied on reference regions from within the LABP) for segmenting enhancement in LGE CMR data-sets of AF patients, we illustrated that the cut-off levels employed by other centres may not be usable for clinical studies performed in our centre.ConclusionsThe proposed technique has great potential for successful employment in the AF management within our centre. It provides a highly desirable validation of the LGE CMR technique for AF studies. Inter-centre differences in the CMR acquisition protocol and image analysis strategy inevitably impede the selection of a universally optimal algorithm for segmentation of enhancement in AF studies.

Transcoronary ethanol ablation for incessant ventricular tachycardia: a salvage technique when faced with left ventricular thrombus.

A 77-year-old man with a history of bypass surgery following an anterior myocardial infarction was admitted with a VT storm (Fig. 1A). Coronary angiography revealed occlusion of the left anterior descending (LAD) artery with a patent vein graft to the distal vessel, backfilling the mid-anterior septum. Left ventriculography demonstrated poor left ventricular (LV) systolic function and a calcified apical aneurysm with thrombus (confirmed by contrast echocardiography). LV endocardial mapping was therefore abandoned. Epicardial mapping identified no target. After further shocks and failed medical therapy, endocardial mapping revealed an exit site at the right ventricular septum adjacent to a scar zone and the thrombus within the LV aneurysm (Fig. 2A). The red asterisk marks the site of the best pacemap (Fig. 1B) where the tip of the catheter is on the right side of the interventricular septum. Angiography was performed with the LAD graft (white arrowhead) and the distal LAD (black arrowhead) patent (Fig. 2B). The shaded area denotes the superimposed territory of a mid-LAD septal branch on angiography (Fig. 2A and ​andB).B). An interventional wire was retrogradely advanced into the septal branch of the LAD (black asterisk) that subtended the territory of VT origin (shaded region). A balloon occluded (black arrowhead) the retrograde limb of the LAD with contrast injection confirming the position (white dotted line) (Panel C, Fig. 2). After injection of a single 2mL aliquot of ethanol (dehydrated alcohol, Martindale) over 3 min, final angiographic assessment confirmed occlusion of the retrograde limb of the LAD (Panel D, Fig. 2). Clinical VT was rendered non-inducible. Follow-up at 15 months confirmed no further VT. Transcoronary ethanol ablation represents a viable salvage technique when faced with LV thrombus. Fig. 1 Twelve-lead ECG of ventricular tachycardia (Panel A) and at the site of pacemap match (Panel B) Fig. 2 Fluoroscopic images of best pacemap (red asterisk) at VT exit site on RV side of interventricular septum (Panel A); patent LAD graft (white arrowhead) and distal LAD (black arrowhead) with interventional wire retrogradely inserted into septal branch of ...